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Conservation and Disease

ROBERT M. MAY
Biology Department Princeton University Princeton, New Jersey, 08544USA

In developed countries over the past 50 years and more, a combination of better nutrition, better hygiene, antibiotics and other chemotherapeutic agents, and programs of immunization have almost eradicated morbidity and mortality resulting from infectious diseases. The smallpox virus is now extinct in the wild (and no conservationist mourned this act; our concerns change sign as we move from very large organisms to microorganisms). Scarlet fever and diphtheria, which carried off heroines in so many Victorian novels-and in Victorian real life-are rarely heard of today. Vaccination has removed polio from essentially a l developed countries, l and measles, whooping cough, rubella and other childhood infections seem on the road to local extinction in many. Whereas hookworm and other parasitic infections were endemic in the southern regions of the United States in the early years of this century, most people in developed countries today would react with horror to the thought of harboring a couple of intestinal or other parasites. Although heavy burdens of such parasites continue to afllict many people in developing countries, not the least of the reasons why HIV/AIDS so appalls us, I think, is that in developed countries we have come to believe a life free from any serious effects of viral, bacterial, protozoan or helminth infections is a natural state, to which we have some kind of entitlement. Nothing could be further from the truth. As emphasized by Haldane (1949), infectious diseases have undoubtedly been the main agents of morbidity and mortality (and thus the dominant selective forces) in human populations at least for the past 10,000 years. In combination with malnutrition, infectious diseases are still the main cause of the dramatic differences between survivorship curves in developed and developing countries (Bradley, 1974). To put it another way, current estimates are that 30% of HIV infections go on to produce death from AIDS (although this number may rise as
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Conservation Biology Volume 2, No. 1, March 1988

longer runs of data accumulate) which can be compared with the 30% case-mortality associated with smallpox infections that were, until recently, endemic in most parts of the world. Given the conspicuous role that diseases have played, and in many parts of the world continue to play, in human demography, it is surprising that ecologists have given so little attention to the way diseases may affect the distribution and abundance of other animals and plants. Until recently, for example, ecology textbooks had chapters discussing how vertebrate and invertebrate predators may influence prey abundance, but in most cases you will search the index in vain for mention of infectious diseases. I think this is partly because ecologists find four- and six-legged predators more engaging, partly because pathogenic organisms (like decomposers, another category of organisms neglected by most ecologists) are relatively hard to see and thus to study, and partly because veterinarians and wildlife managers understandably tend to focus on individual sick animals rather than on population aspects of infection. The past few years have, however, seen an upsurge in efforts to document the effects that viral, bacterial, protozoan and helminth infections may have on the distribution and abundance of animal populations in the laboratory and-more importantly-in the field (for reviews, see Anderson and May, 1978, 1979 or Toft, 1986). These studies have many implications for conservation biology, some of which are widely recognized and others not. It therefore seemed a good idea to hold a symposium on Conservation and Disease at the first annual meeting for the Society for Conservation Biology, and to publish the four papers presented at that symposium in this issue of the journal. The first paper, by Marilyn Scott, reviews evidence for the ways in which infectious diseases may influence the ecology of animal populations. In particular, Scott gives

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a sympathetic but critical account of the view held by some wildlife biologists that diseases have little effect on the demography of natural populations. I believe much remains to be learned about how infectious diseases affect the persistence and distribution of animal populations, and that there are likely to be many implications for the design of natural parks and refuge areas. Very generally, many natural systems appear to be held in some rough, long-term balance by the shifting dynamics of prey-predator, plant-herbivore, host-pathogen and other interactions among many different patches. In these circumstances, the dynamical behavior of many populations may be different in a reserve-even a very large reserve-than in the originally larger whole from which the reserve is carved out. The nonlinear nature of host-pathogen associations, with their threshold effects whereby endemic or epidemic infections can be maintained or spread at high host densities but not at low densities, makes these associations especially likely to be affected by changes in spatial scale or other disturbances. One possible explanation for the outbreak of canine distemper among the (last remaining?) population of black-footed ferrets, whose history is recounted by Tom Thorne and Elizabeth Williams, could be that such epidemics came and went among sub-populations, depending on their changing densities, in the pristine mosaic of ferret populations that embraced a fair fraction of North America between the Rocky Mountains and the Great Plains (May, 1986). If this speculation is correct, we could have an example where a disease that may have played a regulatory role among shifting patches in a larger ecosystem becomes an agent of extinction as the host range contracts. Such shifting balances between carnivorous hosts and diseases arise in other situations of interest to conservationists. Thus silver-backed jackal populations on the Serengeti appear to have exhibited an increase in average density (and a contraction of average territory size) over the past few years, followed very recently by a crash that seems to be associated with an infectious disease (probably canine distemper; Moehlman, 1983). Wild dogs on the Serengeti are also known to have suffered from periodic outbreaks of disease during the past 30 years (again probably canine distemper). Human activities,which are ultimately responsible for essentially all conservation problems, can interact with disease agents in subtle ways. In their symposium paper, David Rogers and Sarah Randolph show that the original patterns of settlement by humans in sub-SaharanAfrica had the effect of minimizing contact with tsetse flies (which are vectors for trypanosomiasis),while leaving trypanosomiasis endemic among the original ungulate fauna. These cultural practices not only permitted much of the pre-human ecosystem to persist alongside expanding human settlement, but they also provided a barrier to colonization by Arabs and other early invaders.

European invaders, however, set in train changes that continue to have much greater impact on natural ecosystems, as the interplay between introduced and native herbivores has been altered by changing patterns of settlement and tsetse control. Rogers and Randolph emphasize that trypanosomiasis was, until relatively recently, an important factor in helping to preserve natural ecosystems. Other examples where diseases gwe rise to conflicts of interest between human activities and wildlife are less subtle. Thus thousands of badgers have been gassed in their dens in Britain because they are reservoirs for bovine tuberculosis (TB), which affects the dairy cattle over whose pastures badgers roam at night (Anderson and Trewhella, 1985). Although the exisiting policy is sound from a narrowly epidemiological standpoint, other methods of controlling bovine TB are possible; the bill, however, would tend to be paid by different people. By the same token, when and if rabies is reintroduced into Britain there will be pressures to implement tentative plans for eradicating fox populations in southern Britain (rather than, or as well as, vaccinating dogs and cats), giving another instance where disease poses difficult conflicts of interest for conservation biologists. The problems of disease among small (and often unnaturally crowded) populations in zoos and reserves are familiar, but continue to pose hard questions. These problems may arise from new diseases or from old diseases in new settings. Tourism, or even the presence of researchers, can be a factor in introducing or spreading such infections. As touched on by Thorne and Williams in discussing the program of captive breeding of blackfooted ferrets, the problems of disease in small populations are often exacerbated by the associated genetic impoverishment of the population. More broadly, once it is conceded that infectious diseases are likely to be important agents of natural selection, many fundamental questions about the ecological significance of genetic diversity, and about the effects of population bottlenecks in reducing such diversity, assume new significance for conservation biologists (Hamilton, 1982; May and Anderson, 1983; OBrien et al., 1985; Ralls and Ballou, 1988). The problems of introduced or endemic diseases can sometimes pose uncomfortable ethical questions for researchers studying natural populations. For example, should a study group of chimpanzees in the wild be vaccinated against poliomyelitis, or should a polio outbreak be left to run its natural course? The question (which has arisen in practice) can be further complicated by uncertainties as to whether the infection was introduced by contacts with humans or whether it occurred naturally in such populations. More generally, we can ask whether we should ideally aim to preserve populations in natural association with their parasites

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Consenation and Disease

and pathogens, or whether we should try to keep them -like humans in developed countries-unnaturally free from infectious diseases. This latter question is rarely asked, much less answered. These issues shade into those addressed in the paper by Andy Dobson, who asks whether infectious diseases may provide a sharp tool for deliberately eradicating species that are unwanted invaders. Deliberate or accidental introductions of rats, cats, goats and other animals, particularly to previously isolated islands, have caused much destruction of native flora and fauna, and are responsible for the endangered status of many species. Dobson shows how the epidemiological properties of many viral, bacterial, protozoan or helminth pathogens can make them magic bullets, affecting target species but not others; he also surveys the many precautions that should accompany the use of such weapons. In short, infectious diseases are important in the ecology and biogeography of many species, and they are correspondingly important in conservation biology. We are beginning to understand some, but by no means all, the many biological difficulties that diseases can cause in the preservation of species and the management of reserves. More intractable are the political problems that arise when programs designed to control disease among humans or their livestock result directly or indirectly in the destruction of wildlife. Ethical questions concerning the control or eradication of disease in studied populations or in reserves remain largely unasked, nor can such questions be answered until we have a better undertanding of the ways in which infectious diseases influence individual behavior, population dynamics, community structure, and biogeographical patterns.

Anderson, R. M., and R. M. May. 1979. Population biology of infectious diseases. Nature 280:361-367; 455-461. Anderson, R.M., and R M . Trewhella. 1985. Population d y namics of the badger (Meies meies) and the epidemiology of bovine tuberculosis (Mycobactmurn bouis). Phil Trans Roy S C B310527-381. O Bradley, D. J. 1974. Stability in host-parasite systems. Pages 71-87 in M. B. Usher and M. H. Williamson, editors. Ecologicd Stability. Chapman and Hall, London. Hamilton, W. D. 1982. Pathogens as causes of genetic diversity in their host populations. Pages 269-296 in R M. Anderson iand R. M. May, editors. Population Biology of Infectious D s ease Agents. Springer-Verlag,New York. Haldane, J.B.S. 1949. Disease and evolution. LaRicerca Sci Suppl 19:68-76. May, R. M. 1986. The cautionary tale of the black-footed ferret. Nature 320:13-14. May, R. M. and R. M. Anderson. 1983. Epidemiology and genetics in the coevolution of parasites and hosts. Proc Roy Soc B219:281-3 13. Moehlman, P. D. 1983. Socioecology of silver-backed (and golden jackals). Pages 423-438 in J. F. Eisenberg and D. G. Kleiman, editors. Recent Avances in the Study of Mammalian Behavior. Special Publ. No. 7: Am Soc Mammal. OBrien, S.J., et al. 1985. Genetic basis for species vulnerability in the cheetah. Science 227:1428-1434. Ralls, K, and J. Ballou. 1988. Estimates of lethal equivalents and the cost of inbreeding in mammals. Conservation Biology (in press).
Toft, C.A. 1986. Communities of species with parasitic lifestyles. Pages 445-463 in J. Diamond and T. J. Case, editors. Community Ecology. Harper & Row, New York.

References and Notes


Anderson, R. M., and R. M. May. 1978. Regulation and stability of host-parasite population interactions. J Anim Ecol47:219247; 249-267.

Conservation Biology Volume 2, No. 1, March 1988

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